One‐seventh of the world's adult population, or approximately one billion people, are estimated to have OSA. Over the past four decades, obesity, the main risk factor for OSA, has risen in striking proportion worldwide. In the past 5 years, the WHO estimates global obesity to affect almost two billion adults. A second major risk factor for OSA is advanced age. As the prevalence of the ageing population and obesity increases, the vulnerability towards having OSA increases. In addition to these traditional OSA risk factors, studies of the global population reveal select contributing features and phenotypes, including extreme phenotypes and symptom clusters that deserve further examination. Untreated OSA is associated with significant comorbidities and mortality. These represent a tremendous threat to the individual and global health. Beyond the personal toll, the economic costs of OSA are far‐reaching, affecting the individual, family and society directly and indirectly, in terms of productivity and public safety. A better understanding of the pathophysiology, individual and ethnic similarities and differences is needed to better facilitate management of this chronic disease. In some countries, measures of the OSA disease burden are sparse. As the global burden of OSA and its associated comorbidities are projected to further increase, the infrastructure to diagnose and manage OSA will need to adapt. The use of novel approaches (electronic health records and artificial intelligence) to stratify risk, diagnose and affect treatment are necessary. Together, a unified multi‐disciplinary, multi‐organizational, global approach will be needed to manage this disease.

Acute compartment syndrome (ACS) of the lower leg is a time-sensitive orthopedic emergency that relies heavily on precise clinical findings. Late findings of ACS can lead to limb amputation, contractures, paralysis, multiorgan failure, and death. Hallmark symptoms of ACS include the 6 P’s: pain, poikilothermia, pallor, paresthesia, pulselessness, and paralysis. Suspicion of ACS is confirmed by measurement of intracompartmental pressure of the affected compartment. The definitive treatment of ACS is timely fasciotomy. We review the pathophysiology, common causes, diagnosis, and treatment of this potentially devastating condition.

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The Acute Respiratory Distress Syndrome (ARDS) is a major public health problem and a leading source of morbidity in Intensive Care Units (ICUs). Lung tissue in patients with ARDS is characterized by inflammation, with exuberant neutrophil infiltration, activation and degranulation that is thought to initiate tissue injury through the release of proteases and oxygen radicals. Treatment of ARDS is supportive primarily because the underlying pathophysiology is poorly understood. This gap in knowledge must be addressed in order to identify urgently needed therapies. Recent research efforts in anti-inflammatory drug development have focused on identifying common control points in multiple signaling pathways. The protein kinase C (PKC) serine-threonine kinases are master regulators of proinflammatory signaling hubs, making them attractive therapeutic targets. Pharmacological inhibition of broad spectrum PKC activity and, more importantly, of specific PKC isoforms (as well as deletion of PKCs in mice) exerts protective effects in various experimental models of lung injury. Furthermore, PKC isoforms have been implicated in inflammatory processes that may be involved in the pathophysiologic changes that result in ARDS, including activation of innate immune and endothelial cells, neutrophil trafficking to the lung, regulation of alveolar epithelial barrier functions and control of neutrophil pro-inflammatory and pro-survival signaling. This review focuses on the mechanistic involvement of PKC isoforms in the pathogenesis of ARDS and highlights the potential of developing new therapeutic paradigms based on the selective inhibition (or activation) of specific PKC isoforms.

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OSA risk measured by sMVAP correlates with higher risk for select postoperative complications. Associations are stronger for non-Bariatric surgeries, where preoperative screening for OSA is not routinely performed. Thus, preoperative screening may reduce OSA-related risk for adverse postoperative outcomes.

Study Objectives: Obstructive sleep apnea (OSA) is common in commercial motor vehicle operators (CMVOs); however, polysomnography (PSG), the gold-standard diagnostic test, is expensive and inconvenient for screening. OSA is associated with changes in heart rate and voltage on electrocardiography (EKG). We evaluated the utility of EKG parameters in identifying CMVOs at greater risk for sleepiness-related crashes (apnea-hypopnea index [AHI] ≥ 30 events/h). Methods: In this prospective study of CMVOs, we performed EKGs with concurrent PSG, and calculated the respiratory power index (RPI) on EKG, a surrogate for AHI calculated from PSG. We evaluated the utility of two-stage predictive models using simple clinical measures (age, body mass index [BMI], neck circumference, Epworth Sleepiness Scale score, and the Multi-Variable Apnea Prediction [MVAP] score) in the first stage, followed by RPI in a subset as the second-stage. We assessed area under the receiver operating characteristic curve (AUC), sensitivity, and negative posttest probability (NPTP) for this two-stage approach and for RPI alone. Results:The best-performing model used the MVAP, which combines BMI, age, and sex with three OSA symptoms, in the first stage, followed by RPI in the second. The model yielded an estimated (95% confidence interval) AUC of 0.883 (0.767-0.924), sensitivity of 0.917 (0.706-0.962), and NPTP of 0.034 (0.015-0.133). Predictive characteristics were similar using a model with only BMI as the first-stage screen. Conclusions: A two-stage model that combines BMI or the MVAP score in the first stage, with EKG in the second, had robust discriminatory power to identify severe OSA in CMVOs.

Sepsis, a poorly understood syndrome of disordered inflammation, is the leading cause of death in critically ill patients. Lung injury, in the form of the Acute Respiratory Distress Syndrome (ARDS), is the most common form of organ injury in sepsis. The Heat Shock Response, during which Heat Shock Proteins (HSPs) are expressed, is an endogenous mechanism to protect cells from injury. We have found that the abundance of pulmonary Heat Shock Protein 70 (HSP70) is not increased following cecal ligation and double puncture (CLP), a rat model of sepsis-induced ARDS. Using the HIV-1 Trans-Activator of Transcription (TAT) cell penetrating protein, we enhanced HSP70 protein abundance in the lung. We found that intra-tracheal (IT) administration of HSP70 using the TAT methodology, just after CLP (CLP-TAT-HSP70), when compared to treatment with phosphate buffered saline (PBS) (CLP-PBS), significantly increased HSP70 abundance in the lung 24 and 48 h post surgery. Treatment of septic rats with TAT-HSP70 increased HSP70 abundance in histologically normal and abnormal lung regions. In addition, TAT-HSP70 treatment significantly decreased the levels of Macrophage Inflammatory Protein (MIP) -2 and Cytokine Induced Neutrophil Chemoattractant (CINC) -1 24 h after CLP. TATHSP70 treatment reduced Myeloperoxidase abundance 48 h post-CLP and attenuated histological evidence of inflammation at both 24 and 48 h. Administration of TAT-HSP70 also improved 48 h survival in this rat model of sepsis. Thus, IT administration of TAT-HSP70 increased HSP70 abundance in the lung and attenuated the lung injury. Enhancing pulmonary HSP70 using TAT is a novel potential therapeutic strategy for the treatment of ARDS that will be explored further.